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Emerging studies on the gut-liver axis reveal that microbiota metabolites regulate hepatic PXR through dual mechanisms: (1) Direct ligand-receptor interactions, where secondary bile acids (e.g., 3-keto LCA, DCA) and indole-3-propionic acid (IPA) bind PXR-LBD via hydrogen bonding to induce conformational changes, subsequently upregulating CYP3A4\/ABCB1 expression while inhibiting NF-\u03baB-mediated inflammation and modulating bile acid homeostasis through crosstalk with the farnesoid X receptor (FXR); and (2) Epigenetic reprogramming, wherein short-chain fatty acids (SCFAs) such as butyrate enhance PXR transcription by inhibiting histone deacetylase (HDAC) activity and promoting histone acetylation (e.g., at H3K9\/K14 residues), thereby increasing promoter accessibility. This epigenetic mechanism contrasts with the direct ligand-binding pathway by acting indirectly through chromatin remodeling. Dysregulated PXR signaling underlies bile acid imbalance, mitochondrial dysfunction, and chemoresistance, driving clinical development of interventions including probiotic modulation of LCA\/DCA balance, triptolide-mediated PXR activation, and structure-based PXR-targeted drug design. These findings highlight the microbiota-PXR axis as a critical determinant of drug response heterogeneity and a promising therapeutic target for metabolic liver disorders and refractory malignancies.<\/jats:p>","DOI":"10.3389\/fimmu.2025.1692684","type":"journal-article","created":{"date-parts":[[2025,11,24]],"date-time":"2025-11-24T06:29:24Z","timestamp":1763965764000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":9,"title":["Recent advances in gut microbiota metabolite regulation of hepatic pregnane X 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